MBBS Pharmacology Syllabus

Pharmacology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pharmacology in MBBS, not a summary of it.

1. 1

   General Pharmacology

   5 topics

   • Introduction to pharmacology
     • Definitions
     • Scope
     • Branches of pharmacology
   • Pharmacokinetics
     • Absorption
     • Distribution
     • Metabolism
     • Excretion of drugs
   • Pharmacodynamics
     • Mechanisms of drug action
     • Drug-receptor interactions
     • Dose-response relationships
     • Drug potency
   • Pharmacogenetics and personalized medicine
     • Genetic variation in drug response
     • Pharmacogenomic testing
     • Implications for drug therapy
   • Drug development and regulation
     • Preclinical studies
     • Clinical trials
     • Drug approval process
     • Drug scheduling
2. 2

   Autonomic Nervous System Pharmacology

   4 topics

   • Introduction to autonomic pharmacology
     • Neurotransmitters and receptors in the autonomic nervous system
   • Cholinergic drugs
     • Agonists
     • Antagonists
     • Cholinesterase inhibitors
   • Adrenergic drugs
     • Agonists
     • Antagonists
     • Adrenergic neuron blockers
   • Ganglionic and neuromuscular blocking drugs
     • Mechanism of action
     • Uses
     • Adverse effects
3. 3

   Central Nervous System Pharmacology

   7 topics

   • Introduction to CNS Pharmacology
     • Blood-brain barrier
     • Neurotransmitters in the CNS
     • Receptors in the CNS
   • Sedative-hypnotic Drugs
     • Benzodiazepines
     • Barbiturates
     • Non-benzodiazepine sedative-hypnotics
   • Antiepileptic Drugs
     • Mechanisms of action
     • Classification
     • Therapeutic uses
   • Antipsychotic Drugs
     • Typical antipsychotics
     • Atypical antipsychotics
     • Dopamine receptor antagonists
     • Serotonin-dopamine antagonists
   • Antidepressant Drugs
     • SSRIs
     • TCAs
     • MAOIs
     • Atypical antidepressants
     • Serotonin-norepinephrine reuptake inhibitors (SNRIs)
   • Analgesic and Anti-inflammatory Drugs
     • NSAIDs
     • Opioids
     • Adjuvant analgesics
   • Anxiolytic Drugs
     • Benzodiazepines
     • Buspirone
     • Selective serotonin reuptake inhibitors (SSRIs)
4. 4

   Introduction to cardiovascular pharmacology

   3 topics

   • Hemodynamics
   • Cardiac electrophysiology
   • Regulation of blood pressure
5. 5

   Endocrine Pharmacology

   5 topics

   • Introduction to Endocrine Pharmacology
     • Hormone replacement therapy
     • Hormone antagonists
     • Hormone synthesis inhibitors
   • Thyroid and Antithyroid Drugs
     • Thyroid hormones
     • Antithyroid drugs
     • Iodine preparations
   • Glucocorticoids and Mineralocorticoids
     • Mechanism of action
     • Therapeutic uses
     • Adverse effects
   • Insulin and Oral Hypoglycemic Agents
     • Mechanism of action
     • Classification
     • Therapeutic uses
   • Gonadal Hormones and Contraceptives
     • Estrogens
     • Progestins
     • Androgen receptor antagonists
     • Contraceptive methods
6. 6

   Introduction to chemotherapy

   3 topics

   • Principles of antimicrobial therapy
   • Mechanisms of antimicrobial action
   • Drug resistance
7. 7

   Chemotherapy of Neoplastic Diseases

   3 topics

   • Introduction to cancer chemotherapy
     • Principles of cancer therapy
     • Cell cycle-specific vs. cell cycle-nonspecific drugs
   • Anticancer drugs
     • Alkylating agents
     • Antimetabolites
     • Antitumor antibiotics
     • Mitotic inhibitors
     • Targeted therapies
   • Hormonal therapy
     • Hormone receptor antagonists
     • Aromatase inhibitors
     • Gonadotropin-releasing hormone analogs
8. 8

   Principles of toxicology

   3 topics

   • Mechanisms of toxicity
   • Factors affecting toxicity
   • Toxicokinetics

Pharmacology flashcards for MBBS

25 of 51 cards from the Pharmacology deck — real questions with worked answers.

1. Define pharmacology and distinguish its two main branches, pharmacokinetics and pharmacodynamics.

   Pharmacology is the science of how drugs interact with living systems. Pharmacokinetics describes what the body does to the drug (absorption, distribution, metabolism, excretion), while pharmacodynamics describes what the drug does to the body (mechanism of action and effects).

2. What is the difference between a drug's potency and its efficacy?

   Potency is the amount of drug needed to produce a given effect (lower $EC_{50}$ = more potent), reflecting position on the dose axis. Efficacy ($E_{max}$) is the maximal effect a drug can produce regardless of dose. A drug can be highly potent but have low efficacy.

3. State the four pharmacokinetic processes summarized by the acronym ADME.

   Absorption (drug entry into the bloodstream), Distribution (transfer to tissues), Metabolism (biotransformation, mainly hepatic), and Excretion (elimination, mainly renal).

4. Define bioavailability ($F$) and give its value for an intravenous drug.

   Bioavailability is the fraction of an administered dose reaching the systemic circulation unchanged. $F = \frac{AUC_{oral}}{AUC_{IV}} \times \frac{Dose_{IV}}{Dose_{oral}}$. For an IV drug $F = 1$ (100%) by definition.

5. Write the formula for apparent volume of distribution ($V_d$) and explain what a large $V_d$ implies.

   $$V_d = \frac{\text{Amount of drug in body}}{\text{Plasma drug concentration}}$$ A large $V_d$ implies extensive tissue distribution (e.g., lipophilic drugs), with relatively little drug remaining in plasma.

6. Give the relationship between clearance ($CL$), volume of distribution ($V_d$), and elimination half-life ($t_{1/2}$).

   $$t_{1/2} = \frac{0.693 \times V_d}{CL}$$ Half-life increases with larger $V_d$ and decreases with greater clearance.

7. What distinguishes first-order from zero-order elimination kinetics?

   In first-order kinetics a constant fraction of drug is eliminated per unit time (rate proportional to concentration; constant $t_{1/2}$). In zero-order kinetics a constant amount is eliminated per unit time because enzymes are saturated (e.g., ethanol, phenytoin, aspirin at high doses).

8. How many half-lives are required to reach steady state, and what fraction of steady state is achieved at each?

   Steady state is essentially reached in about 4-5 half-lives. After 1 $t_{1/2}$ = 50%, 2 = 75%, 3 = 87.5%, 4 = 93.75%, 5 = ~97% of steady-state concentration.

9. Write the equation for maintenance dose rate at steady state in terms of clearance and target concentration.

   $$\text{Maintenance dose rate} = \frac{CL \times C_{ss} \times \tau}{F}$$ where $C_{ss}$ is target steady-state concentration, $\tau$ the dosing interval, and $F$ bioavailability.

10. Write the loading dose equation and explain why it is independent of clearance.

    $$\text{Loading dose} = \frac{V_d \times C_{target}}{F}$$ It depends only on volume of distribution because its goal is to fill the distribution volume to the target concentration immediately, not to balance elimination.

11. Distinguish Phase I from Phase II drug metabolism reactions.

    Phase I reactions (oxidation, reduction, hydrolysis; largely cytochrome P450) introduce or unmask functional groups, often making drugs more polar or active/toxic. Phase II reactions are conjugations (glucuronidation, sulfation, acetylation, glutathione) that add endogenous groups to increase water solubility for excretion.

12. What is first-pass metabolism and how can it be avoided?

    First-pass metabolism is presystemic elimination of an orally absorbed drug by the gut wall and liver before reaching systemic circulation, reducing bioavailability. It is bypassed by sublingual, rectal, transdermal, inhalational, or parenteral routes.

13. Define therapeutic index (TI) and write its formula.

    The therapeutic index is a measure of drug safety: $$TI = \frac{TD_{50}}{ED_{50}}$$ (or $\frac{LD_{50}}{ED_{50}}$ in animals). A larger TI indicates a wider safety margin.

14. What is pharmacogenetics, and give a classic example of a polymorphism affecting drug metabolism.

    Pharmacogenetics studies how individual genetic variation influences drug response. Example: polymorphisms in N-acetyltransferase (NAT2) classify patients as slow or fast acetylators of isoniazid; slow acetylators are prone to peripheral neuropathy.

15. How do CYP2D6 polymorphisms affect codeine analgesia?

    Codeine is a prodrug bioactivated to morphine by CYP2D6. Poor metabolizers get little analgesia, while ultrarapid metabolizers produce excess morphine and risk respiratory depression (especially in children/breastfeeding).

16. List the phases of clinical drug development (Phase I-IV) and their primary aims.

    Phase I: small number of healthy volunteers, assesses safety/pharmacokinetics. Phase II: patients, assesses efficacy and dose-finding. Phase III: large randomized controlled trials confirming efficacy and monitoring adverse effects. Phase IV: post-marketing surveillance for rare/long-term effects.

17. Define an orphan drug and a black box warning in drug regulation.

    An orphan drug is one developed to treat a rare disease, granted regulatory incentives. A black box (boxed) warning is the strictest FDA label warning, highlighting serious or life-threatening risks.

18. Compare an agonist, a competitive antagonist, and a non-competitive antagonist in terms of their effect on the dose-response curve.

    An agonist binds and activates a receptor (produces $E_{max}$). A competitive antagonist shifts the agonist curve rightward (increased $EC_{50}$) with unchanged $E_{max}$ (surmountable). A non-competitive antagonist reduces $E_{max}$ (insurmountable) and may not shift $EC_{50}$.

19. What is a partial agonist, and how does it behave in the presence of a full agonist?

    A partial agonist binds a receptor but produces a submaximal response even at full occupancy (lower intrinsic efficacy). In the presence of a full agonist it acts as a competitive antagonist, lowering the overall response toward its own ceiling.

20. Define an inverse agonist.

    An inverse agonist binds the same receptor as an agonist but stabilizes the inactive conformation, producing an effect opposite to the agonist by reducing constitutive (basal) receptor activity.

21. Differentiate the two divisions of the autonomic nervous system by their primary neurotransmitters and dominant effects.

    The sympathetic ('fight or flight') division releases noradrenaline at most target organs (acetylcholine at sweat glands/ganglia). The parasympathetic ('rest and digest') division releases acetylcholine. They generally exert opposing effects to maintain homeostasis.

22. Identify the neurotransmitter and receptor type at each location: autonomic ganglia, parasympathetic effector, sympathetic effector (most), and the skeletal neuromuscular junction.

    Autonomic ganglia: ACh on nicotinic ($N_N$). Parasympathetic effector: ACh on muscarinic. Most sympathetic effectors: noradrenaline on adrenergic ($\alpha/\beta$). Neuromuscular junction: ACh on nicotinic ($N_M$).

23. Contrast the second-messenger pathways of the muscarinic receptor subtypes $M_1/M_3/M_5$ versus $M_2/M_4$.

    $M_1, M_3, M_5$ couple to $G_q$, activating phospholipase C to raise $IP_3$ and $DAG$ (excitatory, smooth muscle/glandular). $M_2, M_4$ couple to $G_i$, inhibiting adenylyl cyclase and lowering cAMP (cardiac slowing).

24. Describe the mechanism and key clinical use of physostigmine versus neostigmine.

    Both are reversible acetylcholinesterase inhibitors that increase synaptic ACh. Physostigmine is a tertiary amine that crosses the blood-brain barrier (used for anticholinergic/atropine toxicity). Neostigmine is a quaternary amine that does not enter the CNS (used for myasthenia gravis and reversal of non-depolarizing blockade).

25. What is the mechanism of organophosphate poisoning and its specific antidote?

    Organophosphates irreversibly inhibit acetylcholinesterase, causing ACh accumulation and a cholinergic crisis (DUMBBELLS/SLUDGE). Treatment: atropine (blocks muscarinic effects) plus pralidoxime (reactivates cholinesterase before 'aging').

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